Activities of post-heparin plasma lipoprotein lipase and hepatic lipase during pregnancy and lactation.

Abstract

Abstract. The marked increase in serum triglyceride (TG) in women during pregnancy and lactation was studied. Hormone concentrations, changes in activities of post‐heparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) were correlated with plasma lipoprotein concentrations. The plasma concentrations of free oestriol, oestradiol and prolactin were estimated, and analyses of very low density lipoprotein triacylgly‐cerol (VLDL‐TG), and low density (LDL‐Chol) and high density lipoprotein cholesterol (HDL‐Chol) were performed. Post‐heparin plasma LPL and H L activities were selectively measured by an immunochemical method. LPL activity was unaltered during pregnancy and immediately after parturition, values ranging from ll.5 ± l.9 to 12.9 ± l.2 µimol free fatty acid (FFA)/ml/h. Eight weeks after parturition LPL activity was increased to 22.1 ± 5.5 µmiol FFA/ml/h. There was a significant negative correlation between LPL activity and VLDL‐TG concentration in plasma (r= ‐0.58; P < 0.01). The mean HL activity was 7.8 ± 1.9 and 6.4 ± 1.5 µxmol FFA/ml/h during mid‐and late pregnancy, respectively, and after parturition the activity increased from 13.5 ± 30 to 32.4 ± 7.5 µol FFA/ml/h in samples taken 3 days and 8 weeks after parturition. In spite of the changes in HL activity no correlation was found between HL activity and the concentrations of plasma lipoprotein lipids. HL activity bore a significant negative correlation with plasma free oestriol (r= ‐0.46; P < 005), oestradiol (r= ‐0.57; P < 001) and prolactin (r= ‐0.76; P < 0001) levels. Since oestrogens are known to reduce HL activity, the increase in plasma HL activity during the postpartum period may be caused by the concomitant fall of plasma oestrogen levels. Plasma HDL‐Chol and LDL‐Chol did not vary despite the considerable changes in oestrogen, prolactin and VLDL‐TG levels and HL activity. The increase in plasma VLDL‐TG concentration during pregnancy occurred concomitantly with the increase in unconjugated plasma oestriol, oestradiol and prolactin levels, but it was not associated with any changes in LPL activity. In the second trimester, LPL activity was 12.9 ± 116 (mean ± SEM) µmol FFA/ml/h, which is about 50% of the activity reported for the corresponding age group of nonpregnant women. Thus, lowered removal capacity by extrahepatic tissues is likely to cause the moderate rise in the VLDL‐TG (0.84 ± 0–17 mmol l‐1, mean ± SEM) in the second trimester. At the 38th week of gestation LPL activity was similar to the level seen in midpregnancy, but still the VLDL‐TG was greatly increased (2.85 ± 0.66 mmol l‐1, mean ± SEM). Both oestradiol and prolactin bore a significant positive correlation with the levels of plasma VLDL‐TG (r= 0.52; P < 001 and r= 0.42; P < 0.05, respectively). The present data suggests that the massive pregnancy associated hypertriglyceridaemia is not caused solely by impaired removal of VLDL‐TG by extrahepatic LPL, but is mainly due to the increased synthesis of VLDL‐TG caused by the increased levels of plasma oestrogens.